SpectraCell Blog

Pharmaceutical medications help millions of Americans cope with clinical symptoms every day, but most are not without side effects. In fact, the side effects of a medication are often worse than the original condition according to many patients. One reason for this is that prescription drugs very often cause nutrient depletions, which manifest clinically in very significant ways. A classic example is coenzyme Q10 deficiency caused by statin medications. Statins block an enzyme that affects cholesterol production, but the same enzyme is needed to manufacture the important antioxidant coenzyme Q10, which is a key nutrient needed for cellular energy metabolism proper heart function. So if you block this enzyme (called HMG-CoA reductase for hydroxyl-3-methylglutaryl coenzyme A, which is why statins are known generically as HMG-CoA reductase inhbitors), you may lower cholesterol, but as a consequence you may cause a coenzyme Q10 deficiency, which can manifest as low energy and muscle pain.

Why is this so common? The reason is simple – the pharmaceutical approach is fundamentally different from the nutrient repletion approach in that medications alter or interrupt metabolic pathways to achieve a clinical result while nutrient repletion supports or helps maintain the optimal function of a metabolic pathway to achieve balance. In general, medications are palliative in that they focus often on the relief of symptoms. Conversely, nutrient repletion is curative and the goal is optimal cellular function of which a side effect is relief of symptoms.

This is not to say that medications have no place in health, but they do have a role in nutrient depletion which can cause the unpleasant and dangerous side effects. Especially in the age of polypharmacy – when people take more than one medication simultaneously (including over the counter meds) – nutrient depletions caused by drugs deserve a closer look. Here are some examples of how medications can deplete micronutrients:

Meds can interrupt endogenous production of a nutrient (statins and CoQ10)

Meds impairs absorption in the gastrointestinal tract (antacids and B12)

Meds can increase urinary excretion of nutrients (diuretics and minerals)

Meds can alter the gut microbiome (antibiotics and vitamin K)

Meds can impairs mitochondrial function and cellular respiration

Adding to the problem is that fact research on drug-induced nutrient depletions is comparatively sparse compared to the giant funding allotted to pharmaceutical development and testing. In addition, there is a lag time between the market introduction of a blockbuster drug and potential nutrient depletion-induced side effect data. An example of this is research in the past decade that implicates antacids (proton-pump inhibitors) as a causative factor in cardiac events due to their tendency to deplete magnesium. The strong link between PPI use and arrhythmias (irregular heartbeat) may be caused by magnesium depletion, which may also explain an increased risk in bone fractures for people on long-term PPI use according to the FDA. Although research on PPI-induced magnesium deficiency emerged in the last few years, PPIs have been widely used in the market since 1990. In some cases, the research on drug-induced nutrient depletions may not emerge for many years after a drug is widely accepted into the market.

If you are taking a medication, have your micronutrient levels tested today.

For more information on drug-induced nutrient depletions associated with statins and antacids, download our nutrient wheels!

When people think of autism and nutrition, the first thing that often comes to mind is food sensitivities, especially given the widespread attention to the impact of certain additives and common triggers (such as wheat or dairy) on that condition.

Even more paramount, is the evidence suggesting that Autism is largely a whole-body disorder in which an individual's biochemistry affects the brain, learning and behavior. Restoring balance within the body through food and nutrients, therefore, becomes essential. The good news is, nutritional deficiencies that are impacting your child’s neurological development can be corrected. The list below includes specific micronutrients suggested to have a role in the development and treatment of autism:

Vitamin A: One cause of autism may be a defect in a retinoid receptor protein (G-alpha protein) that is critical for language processing, attention, and sensory perception. Evidence suggests that natural vitamin A fixes this protein defect in autistics.

Folate: Oral folate therapy can resolve symptoms of autism in some cases, particularly in autistics with genes that impair folate-dependent enzymes.

Glutamine: Blood levels of this amino acid - which acts as a neurotransmitter - are particularly low in autistics. Glutamine also helps prevent leaky gut syndrome, which can exacerbate autistic symptoms.

Vitamin C: Improves symptom severity and sensory motor scores in autistic patients possibly due to interaction with dopamine synthesis; it also has a strong sparing effect on glutathione.

Glutathione & Cysteine: Both are commonly deficient in autistic patients. Low antioxidant status impairs detoxification and methylation processes, and has been linked to neurological symptoms in autism, which is often considered an oxidative stress disorder.

Vitamin B6: Cofactor for the neurotransmitters serotonin and dopamine; conversion of B6 to its active form is compromised in many autistics. Supplementation trials with B6 resulted in better eye contact, improved speech, and fewer self-stimulatory behavior in autistics. Some consider B6 in combination with magnesium to be a breakthrough treatment for autism.

Magnesium: Cofactor for the neurotransmitters that affect social reactions and emotion; autistics have low levels. Magnesium improves the effectiveness of B6 therapy.

Zinc: Eliminates mercury from brain tissue. The zinc/ copper ratio is particularly low in autistic kids, and low zinc impairs metallothionein, a protein that removes heavy metals from the body.

Carnitine: Transports fatty acids into cells. Low carnitine status, a common feature of autism, impairs the ability to use fatty acids for learning and social development.

The longer a child goes with Autism, the harder they are to reach. Evaluate your child's micronutrient status today!

For a copy of SpectraCell's Nutrition Correlation chart on autism, click here.

We’ve all heard the proverbial advice for achieving a healthy body and maintaining our weight: exercise and “eat right.” But for those who really want to delve further into the science behind an enviable metabolism, we offer a list of vitamins with an explanation of their role in the body’s ability to burn fat and build muscle.

Vitamin A: This vitamin is particularly good at regulating how genes are expressed. Although genes do determine to an extent how the body stores or burns fat, our genes are, simply stated, not our destiny. Two persons with the same gene may express it very differently, depending on their individual cellular environment. This is where vitamin A enters the picture. It can actually enhance the expression of certain genes that lower a person’s tendency to store food as fat. If one is vitamin A deficient, s/he may be pre-disposed to storing fat tissue. On the other hand, correcting a vitamin A deficiency may have a different, more positive effect, as studies have indicated that vitamin A may reduce the size of fat cells.

Vitamin E: This micronutrient affects metabolism by inhibiting immature fat cells from developing into mature fat cells, which are more “stubborn,” metabolically speaking. The cumulative effect of this is a reduction in fat storage.

Vitamin B3: Also called niacin, vitamin B3 can increase the hormone adiponectin, which is secreted by fat cells. Adiponectin’s main function is to signal cells to burn fuel. It also has a role in helping muscles use glucose for energy rather than storing it as fat.

Vitamin B5: Some evidence suggests that vitamin B5 (AKA pantothenate or pantothenic acid) might be helpful for weight loss because it has been associated with less hunger when dieting. At the cellular level, vitamin B5 activates the enzyme lipoprotein lipase, which breaks down fat cells.

This list is by no means exhaustive: in fact, there are multiple micronutrient influences on weight loss. These micronutrients work both individually and synergistically, and repletion often promotes clinical benefits throughout the body. It should come as no surprise that micronutrient adequacy also supports heart health and energy levels. Therefore, discovering (then correcting) micronutrient deficiencies becomes a critical first step in improving overall health.

Download our quick reference nutrient wheel for weight management.

Tired of not getting the results you want? Interested in learning how you can improve the efficacy of your weight management routine? Get tested and find out how your micronutrient status stacks up!

Epigenetics – the study of changes in organisms caused by modification of gene expression rather than alteration in the genetic code itself– has gained much attention in recent years. Environmental factors including diet, smoking and stress have been shown to impact gene expression through epigenetic mechanisms. In a recent experiment involving the collaboration of several medical institutions, an experiment was performed on mice to determine how their immunity responded to a typical Western diet. When mice were fed a Western diet, systemic inflammation occurred which was entirely expected. However, what was particularly interesting was that the Western (inflammatory) diet fundamentally changed their immune system. After eating high calorie, low nutrient food, not only did the mice exhibit more systemic inflammation (not surprising), but their white blood cells became programmed to remain hyper-sensitive to inflammatory triggers. The cellular “memory” had changed.Here is how it worked: a gene called NLRP3 (for Nucleotide binding domain Like Receptor Protein) makes a protein that is used by our immune cells to recognize harmful bacteria and viruses. This protein made by the NLRP3 gene recognizes “bad” cell remnants. These can be parts of bacterial cell membranes, or pieces of genetic material found in viruses, or even parts of a cell that are supposed to be contained but may leak out due to cellular trauma. It is a fundamental way our immune cells recognize something is wrong – bacteria are present or acute tissue damage occurred, for example – and thus launch an inflammatory response to deal with the biological crisis and take care of it. In this study, the immune cells in mice fed a typical Western diet of high-calorie, low nutrient foods launched the same inflammatory response as if an invading bacterial infection were present. Furthermore, the immune cells became hypersensitive so that they continued their inflammatory attack, even when the mice’s diet was returned to normal. In other words, the immune cells responded to a Western diet in the same way it responds to infections. But instead of the infection clearing up, the Western diet seemed to reprogram the immune cells to stay in a perpetual hyperactive state. These results may help explain why chronic inflammation is behind so many lifestyle-related diseases such as heart disease, obesity and diabetes.

Most people assume that standard cholesterol testing offers an adequate assessment of heart disease risk. If you, like many, have never heard of a lipoprotein profile test, you may be surprised to learn that this test assesses an important risk factor called Lipoprotein(a) or Lp(a) (“lipoprotein little a”). Influenced by genetics and strongly linked to heart disease and blood clotting problems, this risk factor unfortunately is NOT part of routine cholesterol tests or standard lipid panels. In fact, lipoprotein(a) is so strongly linked to heart disease, that it is one of the four lipid-related risk factors cited by the National Institutes of Health National Cholesterol Education Program (NCEP) as worthy of monitoring. Unfortunately, Lp(a) has been notoriously difficult to treat pharmacologically, as statins have shown little efficacy in lowering Lp(a) levels.

Why is Lp(a) so harmful?Evidence suggests that Lp(a) may serve as the link between thrombosis and atherosclerosis. Recent clinical studies have implicated Lp(a) as a risk factor for blood clots whether or not atherosclerosis is present. Because Lp(a) is a small, very dense LDL, it can easily penetrate the arterial lining, become oxidized and build plaque, thus contributing to atherosclerosis independent of its thrombotic potential.

How is high Lp(a) treated?

In a recent double-blind, placebo-controlled trial, patients with elevated cholesterol and elevated Lp(a) were divided into two groups, each with 29 people: Group 1 received a statin only and Group 2 received the same statin plus 2 grams/day of L-carnitine, a supplement that plays a key role in fatty acid transport within cells. After 12 weeks, the group receiving only a statin showed about a 7% reduction in Lp(a), but the group receiving the L-carnitine in conjunction with the statin demonstrated over 19% reduction in Lp(a) levels. Authors suggest that co-administration of L-carnitine (whose primary function is fatty acid metabolism), may enhance efforts to lower Lp(a) compared to using a statin alone.

Although heredity plays a large role in the levels of Lp(a), treatment with niacin has also been found to lower levels of Lp(a).

As we stroll into heart month (Feb), still the #1 killer of Americans - 20 years after the declaration to reduce heart-related deaths - here we are. Still. Trying like heck to reduce the risk of heart-related (and other co-morbidities) incidences.

According to statistics from the CDC in 2016, 610,000 heart-related deaths occur each year and it is the leading cause of death in both men and women. That is 1 in 4 Americans.

Why are we still here? After all, we know what we can do: exercise more, take our multivitamin, get regular checks-ups at our doctors' office and - oh yeah - eat more healthfully. Many of us are still sticking to our New Year's Resolutions!

Amid our plight to prepare more healthy home-cooked meals with an eye to consuming higher amounts of plant-based foods, with greater amounts of heart-protecting fiber, healthy, lean proteins, less sugar and processed foods, are we able to keep on with these habits - forever?

Some might say a resounding, "YES!", well, others...maybe...not so much. We have the statistics to prove it.

What do we do if we feel like we have "tried it all", and the results don't appear to be paying off?

What if we have test results, like an advanced lipoprotein or cardiometabolic profile that continue to stare us in the face and prove the errors of our ways? It's disheartening when the labors of our actions appear to be largely ignored by our body's metabolism.

Is it time to finally give up? Should New Year's Resolutions focus on some other aspect, other than finally getting healthy?

Perhaps it is time for a different approach…

The practice of fasting has had many surges over the millennia, extending from times of scarcity, to practices of mystics and religious groups and holidays to health-faddists. Some believed it brought spiritual enlightenment, or quick weight loss; while others believed it gave the digestive system a chance to rejuvenate itself, similar to the idea that adequate nightly sleep allows a reset of the nervous system.

It is largely this last assumption which has pioneered continued research into fasting and its multiple health benefits, including heart (but not limited to) health.1-4

I had the good fortune of learning first-hand about the incredible research into fasting this past December while attending the American Academy of Anti-Aging Medicine in Las Vegas. Valter Longo, PhD, who directs the USC Longevity Institute, expertly presented his research on fasting and its connection to a longer, healthier existence.5 Instead of fasting for long periods of time (4 days to a couple of weeks), the same benefits can be achieved through "Time-Restricted Fasting/Re-feeding" (TRF) or "Fasting-Mimicking Diet" (FMD). Below are two links to fascinating presentations featuring Dr. Longo and his work.

Essentially, with TRF and FMD, an individual can positively impact health for prolonged periods of time simply by choosing to consume all of their daily calories in an 8-hour window. If the first caloric consumption (this includes beverages so no cream or sugar in your coffee) of the day starts at 10:00 AM, an individual is done feeding by 6:00 that evening. If 11:00 is start time, 7:00 is finish time, and so forth.

What does FMD do, exactly?

The Fasting-Mimicking Diet creates the time needed to accomplish an "internal housekeeping" on the cellular level known to stimulate a pathway called: autophagy. Whether you choose to say it "Ah-tauf-ah-gee"or "auto-fay-gee" (I've learned both are right), somatic cells auto-phagocytize, literally eat themselves, to sweep out the debris of aberrant (faulty, damaged or maladapted) cells that build up in our cellular metabolism. Additionally, internal organs, like the heart, all shrink to their reset size, which allows for more effective functioning. When we eat too frequently and don't allow the digestive system to rest, clean and rebuild with re-feeding, autophagy processes are disrupted.

How will autophagy improve my heart health, specifically?As noted earlier, autophagy has profound positive effects on many body systems and functions, as well as cancer prevention and other diseases, but one of the most researched areas in autophagy include cardiovascular disease. Since mitochondria are found in abundance within the cardiac muscle and TRF and FMD precipitate autophagy, another way fasting improves heart health might be through preserving mitochondrial integrity. 6

Dr. Longo's research has also shown that TRF and FMD influences cellular adaptive responses by reducing oxidative damage and inflammation; as well as optimizing energy metabolism and bolstering cellular protection.7

Consider this startling statistic: 50% of people who have heart attacks have "normal" cholesterol. Stated differently, half of all heart attack victims could have a routine cholesterol test done on the very day they have a heart attack and their cholesterol (by routine testing standards) would be "normal" range. So, why do so many practitioners use a diagnostic test that is only 50% accurate? The reason is simple: it’s the test with which they are familiar and have been using for decades. Knowing your HDL and LDL - the "good" and "bad" cholesterol is only the beginning. SpectraCell’s LPP (Lipoprotein Particle Profile) test goes much, much further.

Here is the basic scenario of heart disease: When our blood vessels are "scratched," or injured, plaque builds up in our arteries to repair the injury, sort of like a scab on the inside of the blood vessel, causing reduced blood flow. Since plaque buildup is our bodies' response to injury of the blood vessels, reducing the injury to our arteries is key.

That's where cholesterol comes in. Cholesterol is actually a response to vascular injury - not the cause of it. Cholesterol is really not the culprit. Lipoproteins are. Lipoproteins are what "scratch" or "burrow" into our arteries causing injury. They are actually tiny balls in our blood that carry the cholesterol, our vascular scapegoat. Lipoproteins are what do the damage, not the cholesterol inside them. Cholesterol is really just along for the ride. Lipoproteins, at least the dangerous ones, are the real villain.

There are different sizes of lipoproteins. In general, bigger is better. Here's why: Larger, fluffier LDL particles cannot lodge into your arteries (which is an injury to the artery) as easily as the smaller LDL particles can. Less injury to the artery means less plaque formation and clearer, more pliable blood vessels - a good thing. So it is imperative to understand what kind of LDL (low density lipoproteins) you have floating around in your blood. There are some that are extraordinarily dangerous and some that are completely benign.

For example, RLP (also called remnant lipoprotein) has been cited by the government as a very high risk factor for heart disease. But statins, which lower LDL, will do nothing to help your RLP, which are best lowered by high dose omega 3 fatty acids. So, if you don't know what kind of lipoproteins you have, you're shooting in the dark in terms of what treatments you should take. You can see why measuring just plain old cholesterol is certainly not enough. That is why 50% of the people who have fatal heart attacks have "normal" cholesterol - they are not getting the right cholesterol/ lipoprotein test done.

Here's the best part: SpectraCell's LPP® test costs about the same as an outdated cholesterol test and it is also often covered by insurance. Why wouldn't you want an LPP® done?

Although autism likely has more than a singular cause, it is possible that one nutrient deficiency or imbalance can have a significant impact on its development. Recent evidence suggests that carnitine – a relatively under-recognized nutrient among the general public – plays a bigger role in autism than previously thought.

Carnitine’s main function is to transport fatty acids into the cellular powerhouse (mitochondria) for energy. Low carnitine status (common in autism) can impair the ability to use fatty acids for learning and social development. This recent research hypothesizes that carnitine deficiency may cause symptoms of autism and goes on to suggest that up to 20% of autism cases may be preventable via appropriate supplementation. The author points out that a defect in carnitine biosynthesis is a risk factor for autism, citing the gene (SLC6A14) that limits carnitine utilization in the brain. Expressed only in males, this suggests the reason that autism is more prevalent in boys than in girls.

For additional information about the micronutrient impact on this this condition, download the Nutrients and Autism flyer here.

For more details on the cited paper, click here for a link to the abstract, “Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: a hypothesis,” published in the July 2017 issue of Bioassays.

A vitamin B1 deficiency has been shown to compromise egg cell health in female mice. Even though this study was carried out on mice, the implications for human health and fertility are not lost. Scientists were interested in assessing the effect of mild and severe vitamin B1 (thiamin) deficiency on egg cells and what they found was revealing.

Mice were fed one of two diets: normal or one lacking in vitamin B1. Not surprisingly, the vitamin B1 concentration in the ovaries of mice not given vitamin B1 was much lower than that of mice fed B1. Since the major source of cellular energy in oocytes (immature egg cells) comes from a compound (pyruvic acid) that is metabolized by a vitamin B1-dependent enzyme, researchers wanted to investigate the impact of B1 deficiency on egg cell development.

If the vitamin B1 deficiency was “mild” (not severe enough to cause weight loss), the mice ovaries produced egg cells that were normal. However, if B1 deficiency reached severe levels, then their ovaries would produce abnormal egg cells more often: 44% of eggs from severely deficient animals were abnormal, compared to only 14% of eggs from mice with adequate B1. Furthermore, once the mice returned to a vitamin B1-containing diet, the level of abnormal egg cells dropped from 44% to 23%, suggesting that egg cell damage may occur as the cell matures but not in its immature stage.

For more details on the cited paper, click here for a link to the abstract, “Effects of Mild and Severe Vitamin B1 Deficiencies on the Meiotic Maturation of Mice Oocytes,” published in the March 2017 issue of Nutrition and Metabolic Insights. For a copy of the full paper, click here.

Vitamin K is often regarded as a nutrient for improving heart health, lowering cancer risk, and increasing bone density, but it also appears to improve fitness even in healthy athletes. Like most nutrients, it seems to have quite versatile roles.

In this small study, 26 trained male and female athletes were administered placebo or vitamin K2 supplements for eight weeks while they maintained their regular exercise routines. At the beginning of the study and after eight weeks, each person completed a fitness test on an exercise machine designed to quantify their physical work load, oxygen consumption, respiratory rate, cardiac output, and heart rate.

Vitamin K2 supplementation was associated with a 12% increase in cardiac output (volume of blood that the heart is capable of pumping per beat). The authors suggest that vitamin K2, which has previously been shown to play a role in energy metabolism (especially in tissues with high energy requirements such as skeletal muscle and heart) might be considered in healthy athletes to improve performance.

For more details on the cited paper, click here for a link to the abstract, “Oral Consumption of Vitamin K2 for 8 Weeks Associated With Increased Maximal Cardiac Output During Exercise,” published in the July 2017 issue of Alternative Therapies in Health and Medicine.